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Myocardial injury following ischemia/reperfusion(I/R)is a common clinical scenario in patients suffering from ischemic heart disease.An excessive production of reactive oxygen species(ROS)during the early phase of reperfusion following myocardial ischemia has been proposed to contribute to the reperfusion injury.Paradoxically,the ROS has also been recognized as a trigger of pro-survival signaling pathways mediating cardioprotection at a low level.